Karr Catherine J, Rudra Carole B, Miller Kristin A, Gould Timothy R, Larson Timothy, Sathyanarayana Sheela, Koenig Jane Q
Department of Pediatrics, University of Washington, Seattle, WA 98104, USA.
Environ Res. 2009 Apr;109(3):321-7. doi: 10.1016/j.envres.2008.11.006. Epub 2009 Feb 10.
Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM(2.5) and other metrics of traffic-derived air pollution exposure using a matched case-control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM(2.5) exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO(2) was applied to characterize subject's exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subject's residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mother's education, mother's smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (OR(adj)) and 95% confidence interval per 10 mcg/m(3) increase in lifetime PM(2.5) was 1.14, 0.88-1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (OR(adj) 1.17, 0.95-1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.
很少有研究调查空气污染对婴儿发病的主要原因——急性细支气管炎的影响。我们使用了一个匹配的病例对照数据集来研究PM2.5和其他交通源空气污染暴露指标的影响，该数据集来自华盛顿州普吉特海湾地区1997年至2003年的出生和婴儿住院记录。病例细支气管炎住院日期前7天、30天、60天和终生的平均每日PM2.5暴露量来自社区监测器。应用二氧化氮的区域土地利用回归模型来描述病例住院前一个月和住院前终生平均的受试者暴露情况。还确定了受试者在距离高速公路、主要道路和卡车路线150米范围内的居住距离。我们评估了2604例（83%）病例和23354例（85%）对照，这些病例和对照的信息允许对母亲教育程度、母亲孕期吸烟情况以及婴儿种族/族裔进行调整。条件逻辑回归得出的效应估计显示风险增加幅度非常小，在完全调整模型中，任何暴露指标的风险增加均无统计学意义。总体而言，当仅限于归因于呼吸道合胞病毒（RSV）的细支气管炎病例而非未明确病因的病例时，以及对于更长的暴露窗口，风险估计更强。终生PM2.5每增加10微克/立方米，RSV细支气管炎住院的调整后比值比（ORadj）和95%置信区间为1.14，0.88 - 1.46。居住在距离高速公路150米范围内的婴儿的这种风险也有所升高（ORadj 1.17，0.95 - 1.44）。本研究支持一个正在形成的假设，即慢性交通源颗粒物暴露可能会使细支气管炎风险略有增加，尤其是对于在RSV季节高峰期之前或期间出生的婴儿。未来需要开展研究，以调查阈值效应并捕捉婴儿群体中更大的空间差异变异性。
